Cadmium nitrate decreased the viability of Chinese hamster ovary (CHO) cells in a concentration-dependent manner; 50% inhibition (IC50) was achieved at 0.015 mM. In contrast, lead nitrate appeared to be less toxic. Neither cadmium nitrate nor lead nitrate significantly increased frequencies of binucleated CHO cells with micronuclei (MN). However, both cadmium nitrate and lead nitrate could augment sister chromatid exchanges (SCEs). Cadmium nitrate induced SCEs with a potency approximately equal to that of mitomycin C and more than 10 times higher than lead nitrate. Cadmium nitrate also increased chromosome aberrations (CAs), which included breaks, acentrics, interchanges, and dicentrics of chromosomes. In addition, cadmium nitrate induced a decrease in the mitotic index (MI), but lead nitrate increased it. In summary, it appears that both of these two heavy metal salts have cytogenetic toxicities with different degrees of effects on the cytotoxicity, MN, CAs, and SCEs in CHO cells. However, SCE was the most sensitive endpoint for indicating mutagenetic effects of cadmium and lead in the present study.
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The in vivo effect of E. coli lipopolysaccharide (LPS) on the spontaneous release of transmitter was studied in the isolated phrenic nerve‐diaphragm preparation of the mouse
The resting membrane potential was decreased and frequency of miniature endplate potentials (m.e.p.ps) was increased by treatment with LPS
Pretreatment of diaphragms with ouabain markedly increased the frequency of m.e.p.ps in control group but not in the LPS group
When mice were treated with polymyxin B (a LPS neutralizer), pentoxifylline (an inhibitor of tumour necrosis factor‐α formation) and NG‐nitro‐L‐arginine (an inhibitor of nitric oxide (NO) synthase) the effects of LPS were reversed
These results suggest that LPS increases the spontaneous transmitter release through, at least in part, the pathways of tumour necrosis factor‐α and NO followed by an inhibition of the Na+‐pump activity in the endplate area.
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